Figure 9.
A model for repression of NFκB-mediated activation by glucocorticoid receptor (GR). TNFα treatment induces NFκB response element binding, preinitiation complex assembly, and transcription. Dexamethasone treatment induces tethering of GR to RelA-occupied NFκB response elements. The GR-ligand binding domain, perhaps via recruitment of an unidentified corepressor, bypasses RelA activation domain functions, interfering with phosphorylation of the pol II CTD at serine-2.